Preventive effects of Chinese sumac fruits against acetaminophen-induced liver injury in mice via regulating oxidative stress, inflammation and apoptosis

Abstract

This study aimed to investigate the effects of the phenolic-rich fraction from Chinese sumac fruits against liver injury induced by acetaminophen in mice and elucidate the potential molecular mechanisms. Results showed that the phenolic-rich fraction of the fruits significantly decreased the alanine aminotransferase and aspartate transaminase activities and malondialdehyde content, restored the superoxide dismutase and catalase activities, and reduced the glutathione content. Further analyses revealed that the fraction alleviated liver oxidative stress by upregulating the Nrf2 protein pathway to increase the HO-1 and NQO1 expression levels. It also suppressed liver inflammation by downregulating the expression levels of p-NF-κB, COX-2, p-JNK, p-ERK and p-P38 and inhibiting the secretion of TNF-α, IL-1β, and IL-6. The fraction prevented hepatocyte apoptosis by upregulating p-PI3K, p-Akt, and Bcl-2 and downregulating Bax and cleaved Caspase 3. Thus, the phenolic-rich fraction from Chinese sumac fruits could serve as an adjuvant dietary therapy to prevent drug-induced liver injury.

Keywords

• N-acetyl-p-benzoquinone imine
• Drug-induced liver injury
• Liver damage
• Hepatoprotection
• Reactive oxygen species
• Rhus chinensis Mill